Cardiac Atrial Fibrillation Research Articles

Classification and Recognition of Doppler Ultrasound Images of Patients with Atrial Fibrillation under Machine Learning

This study was aimed to explore the value of the twin neural network model in the classification and recognition of cardiac ultrasound images of patients with atrial fibrillation. 80 patients with cardiac atrial fibrillation were selected and randomly divided into experimental group (40 cases) and control group (40 cases). The twin neural network (TNN) model was combined with traditional ultrasound, Doppler spectrum, tissue velocity, and strain imaging technology to obtain the patient’s cardiac structure parameters and analyze and compare related indicators. The results showed that the total atrial emptying fraction (TA-EF value) of the experimental group was 53.08%, which was significantly lower than that of the control group ( P < 0.05 ). There were no significant differences in left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDD), left atrial maximum volume (LAVmax), and left ventricular ejection fraction (LVEF) between the two groups. In the experimental group, the average peak velocity of mitral valve annulus (Em) was 8.49 cm/s, the peak velocity of lateral wall systole (Vs) was 6.82 cm/s, and the propagation velocity of left ventricular blood flow (Vp) was 51.2 cm/s, which were significantly reduced ( P < 0.05 ). The average values of peak strains in the middle and upper left atrium of the experimental group were significantly lower than those of the control group ( P < 0.05 ). It can be concluded that the combined use of the TNN model can more accurately and quickly classify and recognize ultrasound images.

TRPM7 contributes to progressive nephropathy

TRPM7 belongs to the Transient Receptor Potential Melastatin family of ion channels and is a divalent cation-conducting ion channel fused with a functional kinase. TRPM7 plays a key role in a variety of diseases, including neuronal death in ischemia, cancer, cardiac atrial fibrillation, malaria invasion. TRPM7 is aberrantly over-expressed in lung, liver and heart fibrosis. It is also overexpressed after renal ischemia-reperfusion, an event that induces kidney injury and fibrosis. However, the role of TRPM7 in kidney fibrosis is unclear. Using the unilateral ureteral obstruction (UUO) mouse model, we examined whether TRPM7 contributes to progressive renal damage and fibrosis. We find that TRPM7 expression increases in UUO kidneys. Systemic application of NS8593, a known TRPM7 inhibitor, prevents kidney atrophy in UUO kidneys, retains tubular formation, and reduces TRPM7 expression to normal levels. Cell proliferation of both tubular epithelial cells and interstitial cells is reduced by NS8593 treatment in UUO kidneys, as are TGF-β1/Smad signaling events. We conclude that TRPM7 is upregulated during inflammatory renal damage and propose that pharmacological intervention targeting TRPM7 may prove protective in progressive kidney fibrosis.

An old medicine as a new drug to prevent mitochondrial complex I from producing oxygen radicals.

FindingsHere, we demonstrate that OP2113 (5-(4-Methoxyphenyl)-3H-1,2-dithiole-3-thione, CAS 532-11-6), synthesized and used as a drug since 1696, does not act as an unspecific antioxidant molecule (i.e., as a radical scavenger) but unexpectedly decreases mitochondrial reactive oxygen species (ROS/H2O2) production by acting as a specific inhibitor of ROS production at the IQ site of complex I of the mitochondrial respiratory chain. Studies performed on isolated rat heart mitochondria also showed that OP2113 does not affect oxidative phosphorylation driven by complex I or complex II substrates. We assessed the effect of OP2113 on an infarct model of ex vivo rat heart in which mitochondrial ROS production is highly involved and showed that OP2113 protects heart tissue as well as the recovery of heart contractile activity.Conclusion / SignificanceThis work represents the first demonstration of a drug authorized for use in humans that can prevent mitochondria from producing ROS/H2O2. OP2113 therefore appears to be a member of the new class of mitochondrial ROS blockers (S1QELs) and could protect mitochondrial function in numerous diseases in which ROS-induced mitochondrial dysfunction occurs. These applications include but are not limited to aging, Parkinson’s and Alzheimer's diseases, cardiac atrial fibrillation, and ischemia-reperfusion injury.